1. IntroductionTrichinellosis is a parasitic zoonosis transmitted to humans

through a variety of mammals. Although traditionally herbi-

vores have been considered non-specific hosts, it is now

known that they can participate in the transmission of this

disease to human beings. Thus, outbreaks of trichinellosis inwhich the origin was horsemeat have been reported [3, 12,16, 36]. Furthermore, it has been experimentally proven thatnot only horses [15, 18, 27, 30, 31, 36], but other herbivoressuch as bovine [28 ] or sheep [1, 27, 34] can also be suitablehosts for Trichinella spiralis. In spite of the interest in thistype of research, there are not available data about the beha-viour of other herbivores, such as the goat, with regard toTrichinella spiralis infection. The goat is, probably, the mostimportant livestock species in the Canary Islands, Spain,where this experiment was carried out.

ARTICLE ORIGINAL

Pathological changes in goats experimentallyinfected with Trichinella spiralis*

° D. REINA, °° M.C. MUÑOZ-OJEDA, ° E. PÉREZ-MARTÍN, ° I. NAVARRETE and °°° E. REDONDO*

° Chair of Parasitology. School of Veterinary Medicine, University of Extremadura, 10071 - Cáceres, Spain°° Chair of Internal Medicine, School of Veterinary Medicine, University of Las Palmas, 35016 - Las Palmas de Gran Canaria, Spain

°°° Chair of Pathology, School of Veterinary Medicine, University of Extremadura, 10071 - Cáceres, Spain* Corresponding author : Eloy Redondo, Facultad de Veterinaria, Unidad de Histología y Anatomía Patológica, Avda. Universidad s/n E-10071-Cáceres, Spain

Phone : +34 927 257100 - Fax : +34 927 257110 - Web : http://veterinaria.unex.es - E-mail: eloy@unex.es

SUMMARY

This paper presents the results of a histopathological study carried out in10 autochthonous kids (6 male and 4 female) experimentally infected withTrichinella spiralis "T1" to demonstrate the host character of goats to T. spi-ralis and the alterations produced by the parasite in this atypical host.

Hypertrophia of Peyer's patches, desquamative and catarrhal enteritis thatevolve to hyperplasic and chronic enteritis in the intestine ; glycogen dege-neration and granulomatous hepatitis in the liver ; membranoproliferativeglomerulonephritis, tubular degeneration and interstitial oedema that evol-ve to interstitial nephritis ; hyperemia and interfascicular oedema, Zenkerdegeneration, granulomatous myositis (myocarditis in the heart) and pre-sence of interfibrillar cysts in the striated muscle were the main alterationsobserved. Besides these lesions, others were detected in the spleen, lymphnodes, lungs and central nervous system.

This extensive lesional picture, and the excellent establishment of T. spi-ralis larvae in the musculature confirm the host character of the goats to theparasite.

KEY-WORDS : Trichinella spiralis - experimental infec-tion - pathology - goats.

RÉSUMÉ

Infestation expérimentale des chèvres par Trichinella spiralis : lésionshistopathologiques. Par D. REINA, M.C. MUÑOZ-OJEDA, E.PÉREZ-MARTÍN, I. NAVARRETE et E. REDONDO.

Ce travail présente les résultats d'une étude histopathologique réaliséechez 10 chevraux (6 mâles et 4 femelles) infestés expérimentalement parTrichinella spiralis "T1" afin d'étudier ses pouvoirs infestant et pathogènechez cet hôte atypique.

Dans l'intestin on a observé une hypertrophie des plaques de Peyer, uneentérite évoluant en entérite hyperplasique chronique. Dans le foie, les prin-cipales lésions observées furent une dégénérescence glycogénique et unehépatite granulomateuse. Le rein a montré principalement une glomérulo-néphrite membrano-proliférative, une dégénérescence tubulaire et unœdème interstitiel évoluant en néphrite interstitielle. Dans les muscles, on amis en évidence des signes d'hyperémie et d'œdème, une dégénérescence deZenker, une myosite granulomateuse avec myocardite et la présence dekystes parasitaires. D'autres lésions ont pu être observées dans la rate, lesnodules lymphatiques, les poumons ou le système nerveux central.

MOTS-CLÉS : Trichinella spiralis - infection expérimen-tale - pathologie - chèvres.

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* This project was funded by the Ministerio de Sanidad of Spain(DGICYT • FISS •, Project No. 92/0589).

As indicator of the establishment of Trichinella sp. in thisatypical host, the present paper shows the description of thepathological effects of this parasite in the goat.

2. Materials and methodsA) ANIMALS

A total of 10 goats (six males and four females), twomonths old and about 10 kg body weight were used in thisexperiment, according with a previous paper [22].

B) PARASITEThe experiment was carried out using a synanthropic iso-

late of Trichinella spiralis as infecting material [22], obtai-ned from domestic pigs and typified according to the Interna-tional Commission on Trichinellosis (ICT) as "T1" [19].

C) EXPERIMENTAL DESING AND SAMPLE COLLEC-TION

The animals were divided into the following groups :

Group 1 : Eight experimental animals, infected with 1,000larvae kg-1 body weight (approx. 10,000 larvae per animal),"per os" administration of infected muscle tissue from SwissNBC mice.

Group 2 : Two non infected animals, used as control andhoused in the same experimental conditions.

Animals of group 1 were painlessly killed at 5, 7, 20, 30,45, 60 and 90 days post infection (dpi). One animal, pro-grammed to be sacrificed on day 75 pi died on day 23 pi, pos-sibly due to a special and individual susceptibility. This chro-nological period was established according to the duration ofthe biological cycle phases of T. spiralis and for studying thelesions produced. The animals of group 2 (control group)were killed on days 20 and 90 pi.

After sacrifice, the animals were necropsied and samplesfrom abomasum, small and large intestine, skeletal muscles,myocardium, liver, kidney, spleen, lymph nodes, lung andcentral nervous system were taken in order to analyse theanatomopathological and histopathological changes. Thesesamples were fixed in 10 % neutral buffered formalin andabsolute ethanol during 24 hours, embedded in paraffin, sec-tioned at 2-3 µm and stained with hematoxylin and eosin forlight microscopy findings.

3. ResultsNo clinical or pathological abnormalities were observed in

the animals of group two.

The animals of group one, showed an extensive lesionalpicture. The gross examination of the intestine of animalssacrificed on days 5 and 8 pi revealed a moderate congestiveappearance with mucous fluid and a pronounced hyperthropyof Peyer's patches. These lesions were clearly evident fromday 20 pi and became so strong that caused relieves on theileo-cecal mucosal at the end of the experiment (45-90 dpi).

A desquamative catarrhal enteritis (Fig. 1) was microsco-pically observed in the animals necropsied on days 5 and 8 pi,which evolved with decreasing intensity until day 30 pi.Hyperplasic and chronic enteritis (Fig. 2), moderate on days30 and 45 pi and clearly manifest on days 60 and 90 pi, wasobserved. These lesions are characterised by a lymphoidhyperplasia and a very strong reticulohistiocytosis.

Macroscopically, the intestinal smooth muscle showed acongestive appearance. Microscopically, hyperemia andoedema were detected. These lesions were very strong duringthe first days of the experiment, diminishing slowly until day45 pi and, finally, disappeared in the animals sacrificed ondays 60 and 90 pi. Likewise, myofibrolisis and simple myo-sitis appeared after day 45 pi, maintaining their intensity untilthe end of the experiment (Fig. 3).

In the samples taken from the diaphragm, masseters,tongue, intercostal and limb flexor and extensor muscles, aconsiderable congestion was observed in the initial phases ofthe disease (20 dpi), similar to the aforementioned in thesmooth muscle. After day 40 pi and more clearly on day 90 pi, degenerative areas with a whitish appearance could befound in the diaphragm. On a microscopic level, a vascularreaction was observed after day 5 pi, characterised by hyper-emia and interfascicular oedema, which remain strong at day8 pi, moderate at days 20 and 23 pi, slight at days 30 and 45 pi, and then disappeared. In this tissue a simple myositiswas observed, which followed a similar evolution patternafter the day 20 pi. From this date, Zenker degeneration wasfound, which progressively increased until the end of theexperiment (Fig 4). From day 30 pi on, this degenerationcoincided with the appearance of myofibrilar lysis, whoseintensity runs parallel to the degeneration. The same evolu-tion could be observed in the chronic inflammatory reac-tions, firstly detected as a granulomatous process, whichbecame very strong at the end of the experiment (Fig. 5). Thepresence of intrafibrilar parasitic cysts after day 20 pi shouldbe underlined. They were few in number and not wholely for-med on this date, but increased in number and developmentafter days 23 and 45 pi.

In the heart, congestive areas on the surface of the epicar-dium were detected after the first days of the experiment untilday 30 pi. After day 45 pi, they became degeneratives, with awhitish appearance. The most obvious microscopic lesionswere only observed in the vascular processes (hyperemia andoedema) and in the myositic ones. Initially, this myositisappeared as simple myocarditis progressing between days 5 and 30 pi. After day 45 pi, it turned into granulomatousmyositis which reached its maximum expression on day 90 pi(Fig. 6).

Macroscopically, the liver appeared swollen, globate, withslightly discoloured edges which gives it a degenerate aspect.This is confirmed by the microscopic observation of a mode-rate microvascular glycogen degeneration on the first sacrifi-ced animal (Fig. 7). This lesion was clear throughout theexperiment with little variation in intensity. Furthermore, it isworth to mention the existence of a light granulomatoushepatitis formed by mononuclear cells on day 45 pi, withstronger symptoms in the goat sacrificed on day 60 pi, andeven stronger in the one of day 90 pi (Fig. 8).

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PATHOLOGICAL CHANGES IN GOATS EXPERIMENTALLY INFECTED WITH TRICHINELLA SPIRALIS 339

FIGURE 1. — Desquamative enteritis ; (8DPI), x 250. FIGURE 2. — Hyperplasic and chronic enteritis (44 DPI), x 180.

FIGURE 3. — Intestinal smooth muscle. Simple myositis (90 DPI), x 180. FIGURE 4. — Zenker`s degeneration (90 DPI), x 250.

Figure.6 — Granulomatous myocarditis (90 DPI), 180.FIGURE 5. — Parasitic cysts. Granulomatous reaction (44 DPI), x 250.

The kidneys showed alterations which affected not only theglomerulus but also the interstice and tubular system.Macroscopically, until day 30 pi the kidneys looked spheri-cal, with cortical hemorrhages, and the medulla strong incolour. Its decapsulation occurred easily. After day 40 pi thecapsule was strongly attached to the parenchyma and therewas no evidence of hemorrhages. Microscopically, at 5-8 dpia minimal glomerulonephritis was detected. At 20-30 dpi, theglomerulonephritis was membranous, becoming proliferativeafter this date (Fig. 9). In the tubular system, and after 8 dpi,there was a tubular degeneration, which steadily increases inintensity until the final days of the experiment. As a result ofthis degeneration, which includes desquamation of epithelialcells, from day 30 pi on a progressive and evident tubularnecrosis appeared (Fig. 10).

The presence of oedema was evident at the interstitial tis-sue, being moderate on day 5 pi, stronger from day 8 pi to day30 pi. After day 45 pi, the oedema was replaced by a lym-phoplasmocellular infiltration, showing an interstitial nephri-tis, which increased until the end of the experiment (Fig. 11).

Macroscopically, the spleen showed a splenomegalia withconsiderable congestion, from the beginning of the experi-ment until day 30 pi. Likewise, it appeared whitish due to thespreading of the white spleen pulp, which rose in intensityparallel to the experimental process. Microscopically, ahyperplasic reactive splenitis was detected, being acute untilday 30 pi., with a strong vascular stasis due to the spreadingof the red spleen pulp. In the final days it became chronic(Fig. 12) with predominance of white pulp. Furthermore,after day 40 pi, there was lymphocytolysis and reticulohistio-cytosis.

The lymph nodes showed lesions similar to the ones obser-ved in the spleen. A lymphoadenomegalia with oedema wasevident until day 30 pi. The animals sacrificed after this datedidn’t show this oedematous appearance. Microscopically,hyperplasic reactive lymphoadenitis was detected, which wasacute at the beginning of the experiment (Fig. 13) and chro-nic at the end (Fig. 14). A follicular hypertrophy with lym-phocytolysis and reticulohistiocytosis corroborated themacroscopic observations, especially at the end of the expe-riment. The medullar area showed a strong sinusal catarrh(Fig. 15).

During the first phases of the experiment the lungs showeda congestive aspect. However, at the end of the experimentthis organ appeared greyish with signs of hepatization. Also,a marked enlargement of the intra and interlobular septaappeared. Catarrhal bronchitis with mucous secretion andleukocyte infiltration (Fig. 16), as well as a fibrinous bron-chopneumonia, mainly in the cranial lobes, were microscopi-cally observed. Both phenomena were very strong during thefirst days of the cycle (5 and 8 dpi) and progressively dimini-shed to an interseptal cellular infiltrate, constituted by lym-phocytes and histiocytes, after day 20 pi. This interstitialpneumonia, was more acute at the end of the experiment (Fig.17).

Finally, the central nervous system showed a congestiveaspect with wide vessels and presence of fibrin in the ani-mals sacrificed during the first days. At the end of the expe-

riment, it appeared "cooked" and degenerate. Microscopi-cally, hyperemia and moderate perivascular oedema weredetected with dilation of the Virchoff-Robbins areas. Afterday 20 pi an encephalitic reaction was evident, with glia cellsproliferation which placed around the neurone. Also neuro-nophagy phenomena were detected (Fig. 18). This lesionalpicture became more acute at the end of the experiment (days60 and 90 pi).

4. DiscussionConcerning to the outbreaks of human trichinellosis caused

by horsemeat, a large number of researchers have carried outexperimental infections in other herbivores like bovine orsheep (see Introduction). However, none of them have stu-died the alterations that T. spiralis may produce in the organsand tissues of these hosts. Perhaps the only one exceptioncould be the histopathological research in the muscles ofexperimentally infected horses [31, 32]. The present paper is,probably, the first study related to the pathological pictureproduced by Trichinella in herbivores.

Due to the establishment of the new released larvae 1 intothe intestine, the first lesions are evident both at macro andmicroscopic level. Macroscopic observations, such ascongestion and abundant mucous secretion, were previouslydescribed [4, 38]. These organic reactions included themicroscopic evidence of a catarrhal enteritis with cellulardesquamation during at least the first 23 dpi, which were alsodescribed in mice [21, 25], and in dogs [23]. From day 30 today 90 pi, a progressive chronic inflammation occurred, aswell as RACE et al. [21] reported. The inflammation wasalways accompanied by hypertrophy of Peyer's patches, fin-dings previously reported in mice [21], and in dogs [23].These histopathological observations lead us to believe thatthere is a correspondence between the expulsion of the adultsand the evolution of the enteritis. After expulsion, the acutedesquamation became hyperplasic and chronic, while thehypertrophia of Peyer's patches remainded until the end ofthe experiment. These findings could be related with an intes-tinal response to a toxic process produced by the larvae [6].

Before the arrival and establishment of the larvae at themuscles, the first alterations in this tissue became noticeable.So, hyperemia and interfascicular oedema were detected.These alterations were possibly produced by the aforemen-tioned toxic process. Nevertheless, the lesions becameobvious and much more accentuated after the larvae esta-blishment. The main lesions observed were Zenker degenera-tion with intrafibrilar cysts from day 20 pi and granuloma-tous myositis with myofibrolisis from day 30 pi. Theselesions are also described by REINA et al. [23],PROKOPOWICZ et al. [20] and GUTOWSKA et al. [9],which found that the myositis appear very early (8, 10 and14-15 dpi, respectively). However, it is universally acceptedthat there is a radical increase of the muscle lesions after thearrival of the larvae [5]. Coinciding with the findings ofHULÍNSKÁ. et al. [10], at the end of the experiment (90 dpi)we observed a predominance of degenerative lesions in theskeletal muscles of the animals infected with Trichinella sp.

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FIGURE 7. — Glycogen degeneration (90 DPI), x 350.

FIGURE 9. — Endotheliomesangial-proliferative glomerulonephritis(45 DPI), x 350.

FIGURE 11. — Interstitial nephritis (90 DPI), x 350.

FIGURE 10. — Tubular necrosis (45-60 DPI), x 250.

FIGURE 12. — Chronic hyperplasic reactive splenitis. Follicularhypertrophy (45 DPI), x 250.

FIGURE 8. — Granulomatous hepatitis (90 DPI), x 250.

In our study, larvae of first stage were also found in the myo-cardium after day 23 pi, although in a few number. Thelesions observed in this tissue were basically limited to thevascular processes, producing a granulomatous myocarditis,as previously described other researchers in other hosts [17,35].

The presence of glycogen degeneration and small granulo-mas is similar to the ones found by REINA et al. [23] in dogs.With the exception of this paper we have not found otherreference to this particular lesion. However, GABRYEL etal. [7] detected granulomatous infiltrate in mice infected withT. pseudospiralis.

Conversely to the findings of PAMBUCIAN and CIRO-NEAU [14] in rats, macroscopically we did not observehepatomegalia in the experimental goats, merely a slight dif-fuse fading, as external expression of the glycogen degenera-tion.

It seems to be that the membranoproliferative and/or endo-theliomesangial-proliferative glomerulonephritis, as themain kidney lesions caused by Trichinella, are generallyaccepted [7, 33, 38]. The latter authors affirm that, after day22 the first glomerular hypertrophy could be detected andfrom this date the intensity of this process increases, beingvery strong at day 56 pi. These observations coincide mostlywith the evolution of glomerulonephritis observed in thisexperiment.

In the lymph nodes and spleen, hypertrophy has beenreported [2, 7, 38]. This macroscopic observation, due to thereactive and hyperplasic lymphoadenititis and splenitis, ismicroscopically evident at the beginning of the experiment,but acquires strength at the end (after day 45 pi). Followingthe same evolution, we detected follicular hypertrophy, witha loss of lymphocytes and the presence of reticulohistiocyto-sis.

Vascular and inflammatory processes were evident in thelungs, where catarrhal bronchitis was frequently found.Nevertheless, and in spite of previous reports [8, 17, 35], evi-dence of hemorrhagic foci or oedema was not found. On theother hand, coinciding with the findings of these authors, thegoats showed signs of bronchopneumonia which evolved tointerstitial pneumonia with interseptal accumulation of his-tiocytes and lymphocytes.

Like URSELL et al. [35], we found oedema and hyperemiain the central nervous system of our goats. Furthermore, therewas evidence of an encephalitic reaction [35 ]. These fin-dings are in contradiction with the lack of morphologicalalterations described by GABRYEL et al. [7] in the nervoussystem of mice infected with T. pseudospiralis.

Considering all aforementioned alterations, it is possible toconclude that trichinellosis in goats provokes a widespreadinflammatory reaction. The most important lesions are loca-ted in the intestine, liver, kidneys and striated muscles andtheir intensity bear a strict resemblance with the endogenouscycle of the parasite.

The histopathological findings observed in the animals ofthis experiment demonstrate that the goat is a perfect host toT. spiralis. The parasite may complete its biological cycle,

producing some morphological alterations due to its biologi-cal and physiological needs, which are similar to those detec-ted in other more common hosts.

AcknowledgmentsThe authors are very grateful to Mr M. GÓMEZ-

BLÁZQUEZ and Mr G. FERNÁNDEZ for their technicalassistance. Dr M. GARCÍA-ALONSO assisted in the Englishrevision of the manuscript.

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FIGURE 13. — Acute hyperplasic reactive lymphoadenitis (8 DPI), x250.

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PATHOLOGICAL CHANGES IN GOATS EXPERIMENTALLY INFECTED WITH TRICHINELLA SPIRALIS 343

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